Evidence map›Paper›PMID 41898891›Full record

ReviewGenes2026

Exploring the MicroRNA Landscape in Cardiac Amyloidosis: Molecular Insights and Clinical Applications.

Joanna E Kontaraki, Anthoula Plevritaki, Aleksi Sallo, Konstantinos Fragkiadakis, Eleutherios Kallergis, Evangelos Zacharis, John Kopidakis, Emmanouil Kampanieris, Sophia Achladianaki, Vasiliki Papakosta and 2 more

Abstract readReview
In one paragraph

Review in Genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Joanna E KontarakiMolecular Cardiology Laboratory, School of Medicine, University of Crete, 70013 Heraklion, Crete, Greece.ORCID 0000-0003-3160-1856
Anthoula PlevritakiCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.ORCID 0000-0002-8251-5520
Aleksi SalloMolecular Cardiology Laboratory, School of Medicine, University of Crete, 70013 Heraklion, Crete, Greece.ORCID 0009-0001-9772-1896
Konstantinos FragkiadakisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.ORCID 0000-0002-5342-5411
Eleutherios KallergisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.ORCID 0009-0004-5255-2904
Evangelos ZacharisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.
John KopidakisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.
Emmanouil KampanierisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.ORCID 0009-0008-9194-0781
Sophia AchladianakiCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.
Vasiliki PapakostaCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.
Emmanouil SimantirakisCardiology Department, Heraklion University General Hospital, 71500 Heraklion, Crete, Greece.
Maria E MarketouMolecular Cardiology Laboratory, School of Medicine, University of Crete, 70013 Heraklion, Crete, Greece.ORCID 0000-0003-1888-3430

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac amyloidosis (CA) is an increasingly recognized cause of heart failure with preserved ejection fraction, resulting from myocardial deposition of misfolded amyloid fibrils derived predominantly from transthyretin (ATTR wild-type [ATTRwt] or variant [ATTRv]) or immunoglobulin light chains (AL). Despite advances in noninvasive imaging and disease-modifying therapies, delayed diagnosis remains common, and clinically actionable molecular biomarkers for early detection, phenotypic discrimination, and therapeutic monitoring are limited. MicroRNAs (miRNAs), small noncoding regulators of post-transcriptional gene expression, have emerged as key modulators of cardiovascular remodeling and systemic amyloid biology.

methodsWe performed a comprehensive review of experimental, translational, and clinical studies to evaluate the role of miRNAs in transthyretin and light-chain cardiac amyloidosis, incorporating data from myocardial tissue analyses, circulating miRNA profiling, and mechanistic studies in cellular and animal models.

resultsDysregulated miRNA networks contribute to amyloid-induced cardiac injury by modulating mitochondrial energetics, oxidative stress, inflammation, fibrosis, proteostasis, and neurocardiac signaling. Specific miRNAs, including members of the miR-21, miR-29, and miR-30 families, as well as miR-150-5p and miR-339, have been associated with amyloid burden, adverse myocardial remodeling, plasma cell biology, and disease severity. Distinct circulating and tissue miRNA signatures differentiate transthyretin from light-chain cardiac amyloidosis and correlate with functional status, heart failure biomarkers, and clinical outcomes.

conclusionsMiRNAs represent promising diagnostic and prognostic biomarkers in cardiac amyloidosis and offer mechanistic insights into disease pathogenesis. Integration of miRNA profiling with multimodality imaging and emerging RNA-based therapeutics may enable earlier diagnosis and support precision management of amyloid-related heart failure.

Indexed as

AmyloidosisCardiomyopathiesMicroRNAsAnimalsBiomarkersHeart FailureHumansMyocardiumPrealbuminBiomarkersMicroRNAsPrealbumincardiac amyloidosisimmunoglobulin light chainsmicroRNAstransthyretin

Identifiers

PMID41898891
PMCPMC13027005

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.